Goals of this study were to identify and characterize effects of neurokinin A (NKA) in isolated guinea pig hearts. Bradycardia, augmentation of ventricular contractions, and reduction of perfusion pressure were prominent responses to bolus injections of NKA (0.25-25 nmol). NKA was more potent than substance P (SP) in causing bradycardia but did not differ in potency for lowering perfusion pressure. Doses of SP of 25 nmol or less decreased ventricular force, whereas 100 nmol caused a biphasic response. The percent decrease in heart rate produced by 25 nmol NKA was reduced from 58.0 ± 4.8 to 39.6 ± 3.5% in the presence of μM atropine (n = 5). The positive inotropic response to 25 nmol of NKA in spontaneously beating hearts was replaced by a negative inotropic response during pacing (22.5 ± 3.3% increase vs. 11.7 ± 1.7% decrease, n = 5). Reserpine pretreatment did not affect the positive inotropic response to NKA. Specific binding sites for (125)I-labeled NKA were localized to intracardiac ganglia and coronary arteries but not to myocardium. It was concluded that 1) negative chronotropic responses to NKA involve cholinergic and noncholinergic mechanisms, and 2) the positive inotropic response is an indirect action.

Fragmented QRS (fQRS) is a marker of conduction block due to myocardial scar that presents in electrocardiography (ECG) as an additional one or more R wave (R') or notching in the S wave nadir in contiguous leads. However, fQRS description on premature ventricular contractions (PVCs) has not been previously described. We describe a case of a 67-year-old male with a past medical history of prediabetes, hypertension and coronary artery disease who presented after an ophthalmic procedure with asymptomatic PVCs and episodes of bigeminy. Initial ECG showed an isolated fQRS in V2. However, during PVCs significant extrasystoles fragmentation was seen in other coronary territories. Upon reviewing his most recent cardiac catheterization, it showed a 40% ostial and 70% distal left anterior descending stenosis with a mid-segment patent stent, 95% first diagonal stenosis and totally occluded proximal right coronary artery. Identification of diffuse fQRS known to be associated with myocardial scar, sustained arrhythmic events and sudden cardiac death, particularly when seen in the inferior leads, became extremely relevant in our patient. We noted that ejection fraction reduction from 52% to 34% on his last coronary intervention was crucial to decide if an implantable cardioverter-defibrillator would be needed. PVC fragmentation might be a new ECG marker that could uncover both scar and arrhythmia potential in patients at risk of adverse cardiac events.

Background The canine cardiac system has been the model against which many Class III cardiac devices are validated. Thus, it is expected that the canine heart has very similar electrical model to that found in humans. In 1999, the absence of Heart Rate Turbulence (HRT) after a single Pre-Ventricular Contraction (PVC) was linked to high-risk patient after acute myocardial infarction. Studies of HRT were performed on high-risk patients with Holter-Monitors as were most subsequent HRT studies. If HRT could potentially be used as a risk factor of heart disease, it is interesting to study whether HRT is present following a PVC in otherwise healthy canines. Methods For multiple months, five non-medicated, healthy canines were chronically monitored from between 1 and 8 sessions each. At each session, the canines were ventricularly paced to induce PVCs. Electrical signals, as seen through both a right-ventricular lead and Electrocardiogram (ECG) signals, were captured and analyzed to determine whether the canines displayed HRT following each induced PVC. As a contrasting data set, for the majority of the canines, data was also collected once the canines were sedated. Results HRT was noted in all non-medicated and healthy canines. Of the two factors of HRT (slope and onset), TS was the most prominent indicator of HRT. In each canine, the slope was far greater than the 2.5 ms per RR interval threshold varying from 9.8 to 68.8 ms per RR interval. The onset was marked as HRT (onset less than 0%) in 22 of the 26 session. Additional data was analyzed for healthy yet medicated canines showed that sedation affected HRT, but that HRT was generally noted. Conclusion The canine model displayed a similar HRT characteristic as humans during normal and parasympathetic inhibited states. The presence of HRT in canines is most reliable when using TS. Further study in this area with naturally occurring PVCs would be of interest.